Evidence map›Paper›PMID 39104205›Full record

ArticleBiomolecules & therapeutics2024

Inhibition of Tumoral VISTA to Overcome TKI Resistance via Downregulation of the AKT/mTOR and JAK2/STAT5 Pathways in Chronic Myeloid Leukemia.

Kexin Ai, Mu Chen, Zhao Liang, Xiangyang Ding, Yang Gao, Honghao Zhang, Suwan Wu, Yanjie He, Yuhua Li

Abstract read
In one paragraph

Article in Biomolecules & therapeutics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Kexin AiDepartment of Hematology, Zhujiang Hospital, Southern Medical University, Guangzhou 510280, China.
Mu ChenDepartment of Hematology, Zhujiang Hospital, Southern Medical University, Guangzhou 510280, China.
Zhao LiangDepartment of Hematology, Zhujiang Hospital, Southern Medical University, Guangzhou 510280, China.
Xiangyang DingDepartment of Hematology, Zhujiang Hospital, Southern Medical University, Guangzhou 510280, China.
Yang GaoDepartment of Hematology, Zhujiang Hospital, Southern Medical University, Guangzhou 510280, China.
Honghao ZhangDepartment of Hematology, Zhujiang Hospital, Southern Medical University, Guangzhou 510280, China.
Suwan WuDepartment of Hematology, Zhujiang Hospital, Southern Medical University, Guangzhou 510280, China.
Yanjie HeDepartment of Hematology, Zhujiang Hospital, Southern Medical University, Guangzhou 510280, China.
Yuhua LiDepartment of Hematology, Zhujiang Hospital, Southern Medical University, Guangzhou 510280, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tyrosine kinase inhibitors (TKIs) have revolutionized the treatment landscape for chronic myeloid leukemia (CML). However, TKI resistance poses a significant challenge, leading to treatment failure and disease progression. Resistance mechanisms include both BCR::ABL1-dependent and BCR::ABL1-independent pathways. The mechanisms underlying BCR::ABL1 independence remain incompletely understood, with CML cells potentially activating alternative signaling pathways, including the AKT/mTOR and JAK2/STAT5 pathways, to compensate for the loss of BCR::ABL1 kinase activity. This study explored tumoral VISTA (encoded by VSIR) as a contributing factor to TKI resistance in CML patients and identified elevated tumoral VISTA levels as a marker of resistance and poor survival. Through

Indexed as

Chronic myeloid leukemiaNSC-622608TKI resistanceTumoral VISTA

Identifiers

PMID39104205
PMCPMC11392669

What Socratic holds

Textmetadata
LicenceCC BY-NC
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.